See the following:
Book-chapter with mouse examples
Mutant p53 drives pancreatic cancer metastasis through cell-autonomous PDGF receptor beta signaling
Sustained Expression of Mutant p53 is Required for the Invasive Phenotype of Pancreatic Cancer Cells
"Genetically engineered mouse models of pancreatic cancer harboring a latent oncogenic Kras allele (lox-stop-lox KrasG12D), a latent mutant p53R172H, and a tissue specific Cre recombinase (Pdx1-Cre), also known as KPC mice, develop highly metastatic pancreatic cancer that faithfully mimics the human disease (Hingorani et al., 2005). To understand the impact of p53 mutations on cell invasion and metastasis in this well-defined genetic system, we employed a murine KPC pancreatic cancer cell line that lost the remaining p53 wild type allele during disease progression (Morton et al., 2010). The behavior of KPC cell lines stably expressing shRNAs targeting (mutant) p53, or control shRNAs targeting Renilla (KPC+sh.Ctrl), were compared to one another and to a p53-null KPflC cell line (from a Pdx-Cre, LSL-KrasG12D/+, LSL-p53loxP/+) expressing the control shRNA (KPflC+sh.Ctrl)".
A Story of Discovery: KRAS Mouse Model Advances Pancreatic Cancer Research
Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer